Innate immune (e.g., inflammatory) cells are activated early after allograft transplant and are active long term, inducing transplant vasculopathy, a leading cause of late transplant loss. Treatment of transplant vasculopathy remains limited and there is a need for treatments to prevent transplant loss. The connective tissue matrix, specifically, glycosaminoglycans (GAGs) in the endothelial glycocalyx, induce inflammatory cell activation through chemokine binding to form a signal array to attract monocytes and T cells. GAGs are thought to direct chemokine mediated cell migration. Current treatments to reduce allograft organ rejection target the host or recipient T cell and B cell mediated immune responses, but do not prevent inflammatory macrophage reactions driving chronic rejection. Alternative strategies to prevent or reduce transplant rejection are needed.